microRNA-625 inhibits tumorigenicity by suppressing proliferation, migration and invasion in malignant melanoma
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Wei Fang1,3,*, Yibin Fan6,*, Zhenzong Fa1,*, Jinhua Xu3, Hongyu Yu4, Pu Li5, Julin Gu1,2
1Shanghai Key Laboratory of Molecular Medical Mycology, Department of Dermatology and Venereology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China
2Department of Dermatology, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, 201805 China
3Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, 200040, China
4Department of Pathology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China
5Department of Pediatrics, Ruijin Hospital and Ruijin Hospital North, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200025, People’s Republic of China
6Department of Dermatology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang, 310014, China
*These authors have contributed equally to this work
Pu Li, email: [email protected]
Julin Gu, email: [email protected]
Keywords: malignant melanoma, miR-625, tumorigenesis, SOX2
Received: July 29, 2016 Accepted: December 12, 2016 Published: January 18, 2017
Dysregulated microRNA (miR)-625 expression has been observed in several kinds of cancer. MicroRNAs are important factors in the development and progression of malignant melanoma, though the clinical significance and function of miR-625 in human malignant melanoma remain unclear. Levels of miR-625 expression were therefore determined in 36 pairs of malignant melanoma and adjacent non-tumor tissue using qPCR. The effects of miR-625 dysregulation on malignant melanoma cell proliferation, wound healing, migration and invasion in vitro and tumorigenicity in vivo were investigated using CCK-8, transwell assays, and a nude mouse subcutaneous tumor model. Bioinformatics analysis and luciferase reporter system were used to predict and confirm the target gene of miR-625. miR-625 levels were frequently decreased in malignant melanoma. Ectopic expression of miR-625 suppressed proliferation, wound healing, migration, and tumorgenicity in malignant melanoma. Moreover, miR-625 acted, at least in part, by suppressing potential target SOX2. These results show that miR-625 is a tumor suppressor that inhibits the development and progression of malignant melanoma, which suggests miR-625 is potentially a new diagnostic marker and therapeutic target of malignant melanoma.
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